Anorexia and bulimia nervosa are often chronic disorders with some of the highest mortality rates (.10%) of any psychiatric illness. Greater understanding of the etiology of disordered eating attitudes and behaviors that underlie these sometimes fatal disorders will inform intervention and prevention efforts aimed at their amelioration. The primary purpose of the proposed study is to examine the etiology significance of ovarian hormones in the development of eating attitudes and behaviors by examining phenotypic and genetic relationships between eating pathology and basal estrogen and progesterone levels in a community-based sample of twins. A secondary aim is to examine phenotypic and genetic relationships between the stress hormone cortisol and disordered eating variables. Estrogen is expected to show positive relationships with dietary restraint, weight preoccupation, and eating/weight./body concerns, and negative associations with binge eating and compensatory behaviors. Progesterone is expected to attenuate these relationships, such that lower estrogen: progesterone ratios will be associated with increased binge eating and compensatory behaviors, and decreased dietary restraint and associated attitudes. Cortisol is expected to show significant positive relationships with all forms of disordered eating. Common genetic factors are expected to contribute significantly to all of these hormone/disordered eating phenotypic relationships. Participants will include 50 female dizygotic twins recruited from the campus of Michigan State University and surrounding metropolitan areas who will complete self-report questionnaires assessing body dissatisfaction, weight preoccupation, binge eating, compensatory behaviors, eating concerns, and dietary restraint. Early follicular phase salivary hormone concentrations of estradiol, progesterone, and cortisol will be obtained between the hours of 0800 and 0900. Phenotypic associations between eating variables and hormone concentrations will be examined using within-person correlations whereas genetic associations will be examined via cross- twin, cross-trait correlations (i.e., Twin 1,s eating attitudes with Twin 2's hormone levels) and Cholesky Decomposition and model fitting analyses. Understanding the magnitude and nature of genetic associations will increase understanding of the etiology of eating disorders and lead to the potential identification of endogenous risk factors to be explored in genetic and neurobiological research.